ENDOCRINE

By:
Sonny M. Moreno
 Scope

 Physiology
 Disorders
ADH
ADRENAL GLANDS
THYROID
PARATHYROID
PANCREAS
 “The Sequence”
 Hypothalamus
↓
 Pituitary Gland or Hypophysis
Anterior or Adenohypophysis
Posterior or Neurohypophysis
↓
 Target Glands
 APG
 TSH
 ACTH
 ICSH
 FSH
 LH
 MSH
 PROLACTIN
 GH
 PPG
 ADH
 OXYTOCIN
 TARGET GLANDS
 Thyroid
 Adrenal
 Mammary
 Skin
 Bones
 Ovaries
 Testes
 Kidney tubules
 Uterus
 Pancreas
 Alpha – Glucagon - ↑ glucose
 Beta – Insulin - ↓ glucose
 Delta - Somatostatin – growth hormone
 ADH Abnormality

 SIADH
 DI
 SIADH Syndrome of Inappropriate
Anti Diuretic Hormone
 Increased secretion of ADH
 Increased tubular reabsorption
= increased blood volume
(low Hct, hypoosmolality, edema)
 Decreased urine output
= concentrated urine
(high S.G., dark urine)
 Watch out for manifestations of Fluid
Volume Excess
 Caused: over medication of vasopressin and
benign pituitary tumor
 Con’t
 Management:
 FVE intervention
 Stop vasopressin
 Surgery (tumor excision)
 Critical conditions:
 Pulmonary edema
 Cerebral edema
 Heart failure
 Hypertension
 Renal Failure
 DI Diabetes Insipidus

 Decreased ADH secretion

 Decreased tubular reabsorption
= decreased blood volume
(high Hct, hyperosmolality, thrombosis)
 Increased urine output
= diluted urine (low S.G., clear urine)
 Watch out for manifestations of Fluid
Volume Deficit
 Caused: trauma or injury to pituitary gland,
resection of hypophysis, insensitivity of
kidney to ADH
 Con’t
 Management:
 FVD intervention
 Synthetic ADH administration (vasopressin)
 Critical conditions:
 Thrombosis – thromboembolism – pulmonary
embolism
 Ischemia
 Infarction
 Necrosis (CVA, MI, RF)
 ADRENAL GLAND
Abnormality
 Conn’s
 Cushing’s Disease
 Cushing’s Syndrome
 Addison’s Disease
 Pheochromocytoma
 Conn’s Disease or
Primary Hyperaldosteronism

 Adrenal cortex disorder

 Over secretion of aldosterone or mineralocorticoid
 Increased Na and H2O reabsorption=FVE
 Increased K urinary excretion=hypokalemia
 Watch out for manifestations of:
 SIADH
 Hypervolemia or FVE
 Hypokalemia (arrhythmias)
 Caused:
 tumor and trauma of the adrenal cortex
 Con’t
 Management:
 FVE intervention
 Stop sodium intake
 Critical conditions:
 Arrhythmias
 Hypertension
 Same with SIADH
 Cushing’s Disease

 Adrenal cortex disorder

 Over secretion of
 Aldosterone=Na and H2O retention, K excretion
 Glucocorticoid=hyperglycemia
 Androgen
 male:gynecomastia
 female:hoarseness of voice, hirsutism
 Steroids=buffalo neck, trunkal obesity
 Con’t
 Management:
 FVE intervention
 Replace potassium
 Insulin administration
 Hypertension
 Surgery is adrenalectomy
 Critical conditions:
 Arrhythmias due to hypoK
 Hypertensive crisis
 Fluid overload
 Hyperglycemia
 Cushing’s Syndrome

 Pituitary gland disorder

 Same with Cushing’s Disease
 Surgery is hypophysectomy
 Addison’s Disease
 Adrenal cortex disorder
 Hyposecretion of:
 Aldosterone=Na and H2O excretion, K
reabsorption
 Glucocorticoid=hypoglycemia
 Androgen=decreased libido
  MSH=bronzing of the skin (primary)
 Management

 FVD intervention
 Increase potassium excretion
 Glucagon or simple sugar administration
 Steroid medication
 Critical Conditions

 Dehydration
 Arrhythmias due to hyperK
 Hypovolemic shock
 Hypoglycemia
 Same with DI
 Note:
 inc ACTH, inc cortisol = pituitary problem
(benign tumor)
 normal ACTH, inc cortisol = adrenal problem
(benign tumor)
 dec ACTH, dec cortisol = atrophy of the
pituitary gland
 normal ACTH, dec cortisol = atrophy of the
adrenal gland
 Pheochromocytoma

 Hyperfunction of adrenal medulla

 catecholamines (nor E and E)
 S/sx:
 HPN, severe headache, sweat, n&v,
anorexia, dilated pupuls, cold extremities,
CHF and cerebral bleeding.
 Dx

 VMA vanilly mandelic acid (urine

specimen)
 catecholamines (blood specimen)
 blood sugar and glycosuria
 (+) tumor
 Drug of choice (regetine)
 Surgical Intervention (adrenalectomy)
 THYROID GLAND
Abnormality
 Hypothyroidism
 Hyperthyroidism
– Note:
– inc T3, inc T4, dec TSH = thyroid problem
– inc T3, inc T4, inc TSH = pituitary tumor
(benign)
 Hypothyroidism
 Caused by:
 Autoimmune Disease (Hashimoto’s
Thyroiditis)
 Use of radioactive iodine
 Destruction or removal of thyroid tissue
 Dietary iodide deficiency
 Overtreatment of antithyroid drug
 Manifestations

 Fatigue and lethargy

 Weight gain
 Cold hands and feet
 Decreased temp and pulse
 Cold intolerance
 Decreased attention span
 Decreased GIT peristaltic movement
 Constipation
Con’t of s/sx
 SQ swelling, putty skin, putty skin, puffy
eyelids
 Thinning of hair, loss of lateral 1/3 of the
eyebrow
 Menorrhagia or amenorrhea, decreased
libido, abortions
 Myxedema = severe complication leads to
coma
 Management
 Symptomatic
 Thyroid hormone replacement
 T4 Synthroid, Levothyroid
 T3 Cytomel
 T3 & T4 Proloid
 T3 given NGT, faster than T4
 T4 given parenterally (S.E. adrenal insuf.)
 Note: 3-12 wks S/Sx must disappear
 Hyperthyroidism
 Caused by:
 Grave’s Disease
– TSAb thyroid stimulating antibody duplicate
– TSH, which increases thyroid hormone sec.
 Toxic nodular goiter (benign, hot spot)
 Overmedication of thyroid hormone
 Manifestations:
 Nervousness, tremors, emotional lability
 Weight loss, emaciated
 Flushed skin, warm and moist
 Increased temp and palpitation to atrial fib
 Heat intolerance
 Difficulty in sitting quietly
 Thyroid gland may be palpable and a (+) bruit
 Diarrhea
 Bulging eyes (exophthalmus), startled
expression
 Amenorrhea, oligomenorrhea, decreased libido
 Delirium, disorientation, extreme nervousness
 Arrhythmias
 Thyroid storm = hyperpyrexia, diarrhea,
dehydration,
 tachycardia, arrhythmias, delirium, coma, shock,
death
 Surgery:
 SSKI is given preop to dec thyroid vascularity
 Given with juice to disguise taste
 Given with straw to prevent staining of teeth
 Postop:
 Monitor for bleeding
 Check for tetany (parathyroid gland is severed)
 Hoarseness of voice-laryngeal nerve damage
 Watchout thyroid crisis
 Parathyroid Gland
Abnormality
 Hypoparathyroidism
 Hyperparathyroidism
 Hypoparathyroidism
 Caused:
 Accidental removal or destruction of
parthyroid gland Primary
 Thyroidectomy
 Radical neck disection
 Idiopathic
 Autoimmune
 Diagnostic:
 Decreased serum Ca (7.5 mg/100 ml)
 Decreased PTH
 Increased PO4
 Manifestation:
 Hypocalcemia
 Tetany
Chvostek’s sign
Trousseau’s sign
Laryngeal spasm
 Severe anxiety and apprehension
 Management:
 Treat the cause
 IV calcium
Syringe and ampule of Ca sol. on bed
side
 Oral Ca with vit D
 Hyperparathyroidism
 Caused:
 Primary
 adenoma
 hyperplasia
 Diagnostic:
 Increased vit D
 Increased PTH
 Increased serum Ca (11 mg/100 ml)
 Decreased PO4
 Manifestation:
 Hypercalcemia
 Decalcification of bone
 Fracture
 Deep bone pain
 Depression of neuromuscular function
 Generalized fatigue
 Memory loss
 Dec LOC, stupor coma
 Management:
 Treat the cause
 Hydration (IV saline)
 Diuretics (Ca excretion)
 Calcitonin (inhibits bone resorption)
 Dietary Ca restriction
 Avoid thiazide and vit D (may increase Ca)
 Dialysis
 Digitalis is withdrawn (may increase Ca)
 Diabetes Mellitus
 DM is a disorder of glucose
intolerance caused by a
deficiency in insulin
production and action
resulting in hyperglycemia
and abnormal
CHO, CHON and fat metabolism.
 Types
 Type I or IDDM
no insulin
diseased pancreas (beta cell)
 Type II NIDDM
decreased insulin
inadequate insulin
 IDDM
 Genetic and hereditary
 Zero insulin
 Coxsackie virus
 4 P’s with weight loss
 DKA
 NIDDM
 Adult onset
 Genetic
 Insulin resistance
 Obesity
 4 P’s
 HHNKS or HONKS
 Diagnostic Evaluation:
 Fasting Blood Sugar –
 126 mg/dl for 2x NPO 8H
 2H Postprandial Test –
 200 mg/dl
75 gm of sugar orally
then check after 2H
 OGTT - 200 mg/dl
blood is withdrawn
every hour (2H after)
 Random Blood Sugar –
 200 mg/dl
+ 3 P’s blood is withdrawn
anytime
 Glycosylated Hg A1C -
can detect average serum
glucose level over preceding
2-3 months (most reliable)
Adult 2.2%-4.0%
Children 1.8%-4.0%
 About Insulin!
 Hyperinsulinism – tremors, hunger and
diaphoresis will manifest
 Somogyi Phenomenon – rebound hyperglycemia
after insulin administration
(gradual reduction of insulin is the key to manage
it)
 Insulin Pump – external battery operated,
needle is inserted SQ that delivers
regular insulin (monitor hypokalemia)
 Site – abdomen (best site), upper arms,
upper buttocks
 Route – SQ, only REGULAR insulin can be
given as IV bolus
(flush the line first it will absorb insulin)
 Lipodystrophy is a complication if the site
of injection is not rotated properly, it can
also alter the rate of insulin absorption.
 Mixed Insulin – regular (clear) first to be
drawn followed by NPH (cloudy)
 Refrigerate after use.
 IV bolus – mixed with D5W if
hypoglycemic, or PNSS ideal for
DKA and HONKS
 Pinch or 45 for thin patient,
90 for regular client
 Good site must be supple skin.
 TYPES OF INSULIN
ONSET PEAK DURATION
 Immediate Acting 5-25 min, 30-60 min, 5 hour
Lispro
 Short Acting 15-30min, 2-4 hours, 6-8 hours
Humulin R,
Regular,
Semilente
 Intermediate 60-90min, 4-12 hours, 18 hours
Acting
NPH
Lente,
Humulin N
 Long Acting 8 hours, 16-24 hours, 36 hours
Ultra Lente
END